Surfactant phospholipids and proteins are increased in fetal sheep with pulmonary hypertension secondary to fetal systemic arteriovenous fistula

1 Institut National de la Santé et de la Recherche Médicale U492, Faculté de Médecine, Créteil; 2 Maternité, Hôpital Necker-Enfants Malades, Assistance Publique-Hôpitaux de Paris-Université Paris V; and 3 Service de Gynécologie-Obstétrique, Hôpital Rothschild, Assistance Publique-Hôpitaux de Paris-U...

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Published in:American journal of physiology. Lung cellular and molecular physiology 2005-03, Vol.288 (3), p.L562-L568
Main Authors: Benachi, Alexandra, Jouannic, Jean-Marie, Barlier-Mur, Anne-Marie, Chailley-Heu, Bernadette, Bourbon, Jacques R
Format: Article
Language:English
Subjects:
Animals
Arteriovenous Fistula - complications
Arteriovenous Fistula - embryology
Blotting, Western
Carotid Arteries
Disease Models, Animal
DNA - metabolism
Fetal Diseases - metabolism
Fetal Diseases - pathology
Gestational Age
Hypertension, Pulmonary - embryology
Hypertension, Pulmonary - etiology
Hypertension, Pulmonary - metabolism
Jugular Veins
Lung - metabolism
Phospholipids - metabolism
Pulmonary Surfactant-Associated Protein A - metabolism
Pulmonary Surfactant-Associated Protein B - metabolism
Pulmonary Surfactant-Associated Proteins - metabolism
Sheep
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Summary:1 Institut National de la Santé et de la Recherche Médicale U492, Faculté de Médecine, Créteil; 2 Maternité, Hôpital Necker-Enfants Malades, Assistance Publique-Hôpitaux de Paris-Université Paris V; and 3 Service de Gynécologie-Obstétrique, Hôpital Rothschild, Assistance Publique-Hôpitaux de Paris-Université Paris VI, Paris, France Submitted 11 June 2004 ; accepted in final form 17 November 2004 To determine whether prenatal surfactant storage was altered in a model of systemic arteriovenous fistula (SAVF) with pulmonary hypertension, a fistula was created between the internal jugular vein and the carotid artery in 120-day fetal lambs, and surfactant material was explored at 134 days. Total phospholipids (TPL) and disaturated phosphatidylcholine (DSPC) were increased in whole lung tissue. Phospholipid analysis of isolated lamellar body fraction evidenced a specific increase of surfactant pool size: TPL and DSPC in this fraction were enhanced 1.9 and 2.9 times, respectively, when referred to DNA. Although the steady-state level of transcripts of surfactant protein (SP)-A and SP-B was not found to be changed at the time of death, semiquantitative Western blot analysis revealed elevated SP-A and SP-B protein contents three- and twofold, respectively. These findings indicate markedly enhanced accumulation of surfactant material in the presence of surgically induced prenatal pulmonary hypertension. Although total lung cell number was increased by 26%, SP-B immunolabeling indicated that increased surfactant amount did not result from an increased alveolar type II cell proportion, but rather from an increased rate of storage. Whether similar changes in surfactant are encountered in human neonates with persistent pulmonary hypertension is worthy of investigation. fetus; lung surfactant; alveolar type II cells; disaturated phosphatidylcholine Address for reprint requests and other correspondence: A. Benachi, Maternité, Hôpital Necker-Enfants Malades, 149 rue du Sèvres, 75015 Paris, France (E-mail: alexandra.benachi{at}nck.ap-hop-paris.fr )
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.00220.2004